Circulation, Vol 64, 169-175, Copyright © 1981 by American Heart Association
S Swiryn, RA Bauernfeind, CR Wyndham, RC Dhingra, E Palileo, B Strasberg and KM Rosen
The effects of oral disopyramide phosphate on laboratory induction of
paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients
with clinical PSVT. After control electrophysiologic study to determine the
inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/-
45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours
and were then restudied. All patients had inducible, sustained PSVT during
the control study. After disopyramide, PSVT was noninducible in eight
patients (50%), including six of nine with atrioventricular nodal
reentrance and two of seven with atrioventricular reentrance; inducible but
nonsustained in two (12.5%) (both with atrioventricular reentrance); and
inducible and sustained in six (37.5%). The benefit of disopyramide seemed
predominantly to reflect depression of conduction in the retrograde limb of
the circus movements, although effects upon the antegrade limb were also
observed. In the eight patients with inducible PSVT before and after
disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/-
29 msec (mean +/- SEM) (p less than 0.001). These results suggest that
disopyramide would be effective in preventing recurrence of clinical PSVT
in selected patients.
ARTICLES
Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia
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